Th e interferon system represents one of the components of the fi rst line defence against infl uenza virus infection. Interferon omega (IFN-ω) is antigenetically diff erent from IFN-α and IFN-β and can aff ect patients who are resistant to these IFNs. To improve the biological characterization of IFN-ω, we compared its activity with those of type I and type III IFNs in induced A549 cells. Th e antiviral eff ect on IFN-stimulated A549 cells was most apparent aft er infection with avian infl uenza virus. IFN-ω had statistically signifi cant antiviral activity although less than IFN-β1a, IFN-λ1, or IFN-λ2. On the other hand, IFN-ω appeared more effi cient than IFN-α2. Our results also indicate that IFN-λs were more suitable against human highly pathogenic virus. In this case, IFN-λ1 and IFN-λ2 were more potent than type I IFNs.
Type I and type III interferons (IFNs) are induced by viral infection. It was concluded that these IFN species are identical in regulation and biological functions. However, these two systems differ in the tissue expression of their receptors and their transcriptional regulation is fundamentally different as well as cellular signaling pathways that drive expression of each IFN. Here, we have investigated the transcriptional profile of endogenous IFNs after stimulation of cells with exogenous IFNs and subsequent infection of A549 cells with A/chicken/Germany/27 [H7N7] influenza virus. Both type I and type III IFNs exhibit high degree of the cross-induction. Our results show that type III IFNs (IFN-λ1, IFN-λ2 and IFN-λ3) are better inducers of CXCL10 than type I IFNs. The IFN-β1a and IFN-λ2 were the most potent IFNs and they highly increased the level of IFN-α, IFN-β, IFN-λ, and CXCL10 mRNAs. Since type I IFNs up regulated expression of retinoic acid-inducible gene 1 (RIG-1) mRNA, type III IFNs-λ down regulated expression of RIG-1 mRNA in influenza infected cells. IFN-α and IFN-ω induced similar amount of IFN-α, IFN-β and IFN-λ mRNA but differ in induction of CXCL10 and RIG-1 mRNA.
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